Palmer Amaranth (Amaranthus palmeri) is a dicot weed in the Amaranthaceae family. In Mississippi this weed first evolved multiple resistance (to 2 herbicide sites of action) in 2008 and infests Cotton. Multiple resistance has evolved to herbicides in the Groups B/2, and G/9. These particular biotypes are known to have resistance to glyphosate, and pyrithiobac-sodium and they may be cross-resistant to other herbicides in the Groups B/2, and G/9.

The 'Group' letters/numbers that you see throughout this web site refer to the classification of herbicides by their site of action. To see a full list of herbicides and HRAC herbicide classifications click here.

Greenhouse trials comparing a known susceptible Palmer Amaranth biotype with this Palmer Amaranth biotype have been used to confirm resistance. For further information on the tests conducted please contact the local weed scientists that provided this information.

Genetics

Genetic studies on Group B, G/2, 9 resistant Palmer Amaranth have not been reported to the site. There may be a note below or an article discussing the genetics of this biotype in the Fact Sheets and Other Literature

Mechanism of Resistance

The mechanism of resistance for this biotype is either unknown or has not been entered in the database. If you know anything about the mechanism of resistance for this biotype then please update the database.

Relative Fitness

There is no record of differences in fitness or competitiveness of these resistant biotypes when compared to that of normal susceptible biotypes. If you have any information pertaining to the fitness of multiple resistant Palmer Amaranth from Mississippi please update the database.

Research Plant PhysiologistUSDA-ARSCrop Production Systems Research Unit141 Experiment Station RoadStoneville, 38776, MississippiUnited States Email Vijay NandulaWeb : Web Site Link

ACKNOWLEDGEMENTS

The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in Mississippi have been instrumental in providing you this information. Particular thanks is given to Jason Bond, Trey Koger, and Vijay Nandula for providing detailed information.

Greenhouse and laboratory studies were conducted to confirm and quantify glyphosate resistance, quantify pyrithiobac resistance, and investigate interaction between flumiclorac and glyphosate mixtures on control of Palmer amaranth from Mississippi. The GR50 (herbicide dose required to cause a 50% reduction in plant growth) values for two glyphosate-resistant biotypes, C1B1 and T4B1, and a glyphosate-susceptible (GS) biotype were 1.52, 1.3, and 0.09 kg ae ha-1 glyphosate, respectively. This indicated that the C1B1 and T4B1 biotypes were 17- and 14-fold resistant to glyphosate, respectively, compared with the GS biotype. The C1B1 and T4B1 biotypes were also resistant to pyrithiobac, an acetolactate synthase (ALS) inhibitor, with GR50 values of 0.06 and 0.07 kg ai ha-1, respectively. This indicated that the C1B1 and T4B1 biotypes were 7- and 8-fold, respectively, more resistant to pyrithiobac compared with the GS biotype, which had a GR50 value of 0.009 kg ha-1. Flumiclorac was antagonistic to glyphosate by reducing glyphosate translocation. The C1B1 and T4B1 absorbed less glyphosate 48 h after treatment (HAT) compared with the GS biotype. The majority of the translocated glyphosate accumulated in the shoot above the treated leaf (that contains the apical meristem) in the GS biotype and in the shoot below the treated leaf in the resistant biotypes, C1B1 and T4B1, by 48 HAT. The C1B1 biotype accumulated negligible shikimate levels, whereas the T4B1 and GS biotypes recorded elevated levels of shikimate. Metabolism of glyphosate to aminomethylphosphonic acid was not detected in either of the resistant biotypes or the susceptible GS biotype. The above results confirm multiple resistance to glyphosate and pyrithiobac in Palmer amaranth biotypes from Mississippi and indicate that resistance to glyphosate is partly due to reduced absorption and translocation of glyphosate..

BACKGROUND: Palmer amaranth (Amaranthus palmeri S. Wats) is one of the most common and troublesome weeds in the USA. Palmer amaranth resistance to acetolactate synthase (ALS) inhibitors is widespread in the USA, as in Arkansas. The cross-resistance patterns and mechanism of resistance are not known. Experiments were conducted to determine cross-resistance to ALS inhibitors and identify target-site mutations in 20 Palmer amaranth localities from 13 counties in Arkansas.

RESULTS: All Palmer amaranth localities tested had plants cross-resistant to imazethapyr, flumetsulam, primisulfuron, pyrithiobac and trifloxysulfuron. The dose of trifloxysulfuron that caused 50% control was 21–56-fold greater for resis- tant accessions than for susceptible ones. All but three resistant plants analyzed had one or two relative copies of ALS; one plant had seven relative copies. All resistant plants tested (18 localities) carried the Trp574Leu mutation, which is known to confer broad resistance to ALS inhibitors, supporting the cross-resistance pattern observed. Besides the Trp574Leu mutation, 30% of localities had individuals with one additional resistance-conferring mutation including Ala122Thr, Pro197Ala or Ser653Asn.

CONCLUSION: The Trp574Leu mutation in ALS is the primary mechanism of resistance to ALS inhibitors in Palmer amaranth from Arkansas, USA. In some localities, multiple mutations have accumulated in one plant. All localities tested contained plants with resistance to five families of ALS inhibitors. Localities with extremely high resistance to ALS inhibitors, and those outside the subset we studied, may harbor non-target site resistance mechanisms. ALS inhibitors are generally no longer effective on Palmer amaranth in these localities from the US mid-south.

BACKGROUND Herbicide-resistant weeds are a serious problem worldwide. Recently, two populations of Amaranthus palmeri with suspected cross-resistance to acetolactate synthase (ALS)-inhibiting herbicides (R1 and R2) were found by farmers in two locations in Argentina (Vicuña Mackenna and Totoras, respectively). We conducted studies to confirm and elucidate the mechanism of resistance.

RESULTS We performed in vivo dose–response assays, and confirmed that both populations had strong resistance to chlorimuron-ethyl, diclosulam and imazethapyr when compared with a susceptible population (S). In vitro ALS activity inhibition tests only indicated considerable resistance to imazethapyr and chlorimuron-ethyl, indicating that other non-target mechanisms could be involved in diclosulam resistance. Subsequently, molecular analysis of als nucleotide sequences revealed three single base-pair mutations producing substitutions in amino acids previously associated with resistance to ALS inhibitors, A122, W574, and S653.

Resistance to acetolactate synthase (ALS)-inhibitor herbicides due to continuous and repeated
selection is widespread in many troublesome weed species, including Palmer amaranth, throughout
the United States. The objective of this research was to investigate the physiological and molecular
basis of resistance to ALS inhibitors in a chlorsulfuron-resistant Palmer amaranth population (KSR).
Our results indicate that the KSR population exhibits a high level of resistance to chlorsulfuron
compared with two known susceptible populations, MSS and KSS from Mississippi and Kansas,
respectively. MSS is highly susceptible to chlorsulfuron, whereas KSS is moderately sensitive.
Dose–response analysis revealed that KSR was more than 275-fold more resistant compared with
KSS. Nucleotide sequence analysis of the ALS gene from the plants that survived chlorsulfuron
treatment revealed the possibility of evolution of both target site–based and non–target site based
resistance to ALS inhibitors in the KSR population. The most common mutation (Pro-197-Ser) in
the ALS gene associated with resistance to the sulfonylureas in many weed species was found only in
30% of the KSR population. A preliminary malathion study showed that the remaining 70% of resistant
plants might have cytochrome P450–mediated non–target site resistance. This is the first report
elucidating the mechanism of resistance to ALS inhibitors in Palmer amaranth from Kansas. Presence
of both target site– and non–target site based mechanisms of resistance limits the herbicide options
to manage Palmer amaranth in cropping systems..

Transfer of herbicide resistance among closely related weed species is a topic of growing concern. A spiny amaranth × Palmer amaranth hybrid was confirmed resistant to several acetolactate synthase (ALS) inhibitors including imazethapyr, nicosulfuron, pyrithiobac, and trifloxysulfuron. Enzyme assays indicated that the ALS enzyme was insensitive to pyrithiobac and sequencing revealed the presence of a known resistance conferring point mutation, Trp574Leu. Alignment of the ALS gene for Palmer amaranth, spiny amaranth, and putative hybrids revealed the presence of Palmer amaranth ALS sequence in the hybrids rather than spiny amaranth ALS sequences. In addition, sequence upstream of the ALS in the hybrids matched Palmer amaranth and not spiny amaranth. The potential for transfer of ALS inhibitor resistance by hybridization has been demonstrated in the greenhouse and in field experiments. This is the first report of gene transfer for ALS inhibitor resistance documented to occur in the field without artificial/human intervention. These results highlight the need to control related species in both field and surrounding noncrop areas to avoid interspecific transfer of resistance genes..